Verapamil treatment after coronary angioplasty in patients at high risk of recurrent stenosis.

OBJECTIVE--To evaluate the efficacy of high-dose verapamil treatment (240 mg twice daily) in the prevention of angiographic restenosis after primary successful coronary angioplasty in patients at high risk of recurrent obstruction. DESIGN--A placebo controlled, double blind trial in which patients with stable angina pectoris and patients with unstable angina or non-Q wave infarction treated with 330 mg aspirin and 75 mg dipyridamole twice daily were randomised to a verapamil group or a control group. Follow up angiography was performed 6 months after angioplasty or sooner if signs of recurrent ischaemia developed. SETTING--University department of cardiology. PATIENTS--196 consecutive patients undergoing coronary angioplasty from the beginning of April 1987 to the end of March 1989 and meeting the selection criteria that included the presence of at least one of six predefined risk factors for restenosis. At the time of coronary angioplasty 113 patients had unstable angina or non-Q wave infarction and 83 had stable angina pectoris. RESULTS--In 89 (91%) patients in the verapamil group and in 83 (85%) control patients follow up angiograms were available. The restenosis rate was lower in the verapamil group (48.3%) than in the placebo group (62.7%) (odds ratio 0.56, 95% confidence interval (CI) 0.303 to 1.025 p = 0.059). Of the 172 patients in whom follow up angiograms were available, 24 (13 taking verapamil and 11 taking placebo) did not comply with the trial for more than 40 (34) days (mean (1 SD)). For the remaining 148 patients the restenosis rate was 47.4% in the verapamil group and 63.9% in the placebo group (odds ratio 0.52, 95% CI 0.271 to 0.993, p = 0.046). In the 97 patients with unstable angina or non-Q wave infarction the restenosis rate was not significantly influenced by verapamil (55.8% with verapamil v 62.2% with placebo, odds ratio 0.77, 95% CI 0.339 to 1.728, p = 0.520). In the 75 patients with stable angina pectoris the restenosis rate dropped from 63.2% with placebo to 37.8% with verapamil (odds ratio 0.36, 95% CI 0.137 to 0.917, p = 0.038). CONCLUSION--The observed beneficial effect of high-dose verapamil treatment on the angiographic restenosis rate in patients with stable angina pectoris and at increased risk of recurrent obstruction requires confirmation in further prospective studies.

[1]  G. Schuler,et al.  Regular Physical Exercise and Low‐Fat Diet: Effects on Progression of Coronary Artery Disease , 1992, Circulation.

[2]  J. O’Keefe,et al.  Effects of diltiazem on complications and restenosis after coronary angioplasty. , 1991, The American journal of cardiology.

[3]  E. Jones,et al.  Failed elective percutaneous transluminal coronary angioplasty requiring coronary artery bypass surgery. In-hospital and late clinical outcome at 5 years. , 1990, Circulation.

[4]  V. Fuster,et al.  Syndromes of accelerated atherosclerosis: role of vascular injury and smooth muscle cell proliferation. , 1990, Journal of the American College of Cardiology.

[5]  P. Block,et al.  Restenosis after percutaneous transluminal coronary angioplasty--anatomic and pathophysiological mechanisms. Strategies for prevention. , 1990, Circulation.

[6]  P. Serruys,et al.  Restenosis after coronary angioplasty: new standards for clinical studies. , 1990, Journal of the American College of Cardiology.

[7]  Spencer B. King,et al.  Restenosis After Coronary Angioplasty: Potential Biologic Determinants and Role of Intimal Hyperplasia , 1989 .

[8]  W. Vetter,et al.  Ca2+-channel blockers inhibit the action of recombinant platelet-derived growth factor in vascular smooth muscle cells. , 1989, Proceedings of the National Academy of Sciences of the United States of America.

[9]  D. Waters,et al.  Multiple coronary angioplasty: a model to discriminate systemic and procedural factors related to restenosis. , 1988, Journal of the American College of Cardiology.

[10]  C. Jackson,et al.  Inhibitory effect of calcium antagonists on balloon catheter-induced arterial smooth muscle cell proliferation and lesion size. , 1988, Atherosclerosis.

[11]  P W Serruys,et al.  Incidence of restenosis after successful coronary angioplasty: a time-related phenomenon. A quantitative angiographic study in 342 consecutive patients at 1, 2, 3, and 4 months. , 1988, Circulation.

[12]  M. Brand Incidence ofrestenosis after successful coronary angioplasty: a time-related phenomenon , 1988 .

[13]  M. Nobuyoshi,et al.  Restenosis after successful percutaneous transluminal coronary angioplasty: serial angiographic follow-up of 229 patients. , 1988, Journal of the American College of Cardiology.

[14]  O. Stein,et al.  Long‐Term Effects of Verapamil on Aortic Smooth Muscle Cells Cultured in the Presence of Hypercholesterolemic Serum , 1987, Arteriosclerosis.

[15]  B. Chaitman,et al.  Multilesion coronary angioplasty: clinical and angiographic follow-up. , 1987, Journal of the American College of Cardiology.

[16]  S. Mutoh,et al.  Antiatherogenic activity of FR34235 (Nilvadipine), a new potent calcium antagonist. Effect on cuff-induced intimal thickening of rabbit carotid artery. , 1987, Atherosclerosis.

[17]  C. Simpfendorfer,et al.  Frequency, management and follow-up of patients with acute coronary occlusions after percutaneous transluminal coronary angioplasty. , 1987, The American journal of cardiology.

[18]  B. Meier,et al.  Effect of nifedipine on recurrent stenosis after percutaneous transluminal coronary angioplasty. , 1986, Journal of the American College of Cardiology.

[19]  L Morgenstern,et al.  Coronary angioscopy in patients with unstable angina pectoris. , 1986, The New England journal of medicine.

[20]  M. Bertrand,et al.  Comparative results of percutaneous transluminal coronary angioplasty in patients with dynamic versus fixed coronary stenosis. , 1986, Journal of the American College of Cardiology.

[21]  B Meier,et al.  Restenosis after successful coronary angioplasty in patients with single-vessel disease. , 1986, Circulation.

[22]  M. Bourassa,et al.  Clinical and angiographic assessment 6 months after double vessel percutaneous coronary angioplasty. , 1985, Journal of the American College of Cardiology.

[23]  M. Bourassa,et al.  Failure of diltiazem to prevent restenosis after percutaneous transluminal coronary angioplasty. , 1985, American heart journal.

[24]  L. Elveback,et al.  Follow-up clinical results in patients undergoing percutaneous transluminal coronary angioplasty. , 1985, Circulation.

[25]  S Levine,et al.  Coronary angioplasty: clinical and angiographic follow-up. , 1985, The American journal of cardiology.

[26]  C Vallbracht,et al.  Recurrence rate after successful coronary angioplasty. , 1985, European heart journal.

[27]  S. Schwartz,et al.  Significance of Quiescent Smooth Muscle Migration in the Injured Rat Carotid Artery , 1985, Circulation research.

[28]  R E Vlietstra,et al.  Restenosis after percutaneous transluminal coronary angioplasty (PTCA): a report from the PTCA Registry of the National Heart, Lung, and Blood Institute. , 1984, The American journal of cardiology.

[29]  C. Stiles,et al.  Regulation of the Balb/c-3T3 cell cycle-effects of growth factors. , 1980, Journal of supramolecular structure.

[30]  W. Siegenthaler,et al.  Nonoperative dilatation of coronary-artery stenosis: percutaneous transluminal coronary angioplasty. , 1979, The New England journal of medicine.